Abstract

Dysfunction and abnormal differentiation of immune cells and hematopoietic precursors are well described in patients with cancer,although the role of transcription factors in these defects is not well established. Here, we evaluated expression of C/EBP?, PU.1 and BACH1 transcription factors in lymphoid and myeloid cells, including NK cells, T cells, neutrophils and monocytes, isolated from healthy donors and cancer patients

Highlights

  • Cancer remains one of the leading causes of death worldwide despite a significant progress in cancer diagnostics, treatment and prophylactics during last decades

  • Intracellular expression of C/EBPα, PU.1 and BACH1 transcription factors was determined in the peripheral blood NK cells isolated from patients with lung and gastric cancer and healthy donors utilizing specific antibodies and flow cytometry

  • MFI data revealed that the expression of PU.1 transcription factor in NK cells in patients with lung cancer (5.55 ± 0.42) and gastric cancer (5.81 ± 0.32) was significantly reduced compared with the expression of PU.1 in NK cells harvested from healthy volunteers (6.99 ± 0.37) (p

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Summary

Introduction

Cancer remains one of the leading causes of death worldwide despite a significant progress in cancer diagnostics, treatment and prophylactics during last decades. It is generally accepted that the development and progression of cancer are closely associated with dysregulated functioning and diminishing of local and systemic immune responsiveness. The hypothesis of intrinsic transcriptional defects in the differentiation mechanism of hematopoietic stem and progenitor cells as a source of dysfunction of immature and mature immune cells in cancer patients is supported by a growing number of recent findings. A significant reduction in c-myc expression was observed in both NK cells and T lymphocytes in patients with cancer [1,2]. Cancer-associated abnormalities in differentiation of hematopoietic progenitor cells and in myeloid and lymphoid cells have been reported [4,5,6,7]. It is conceivable to speculate that an abnormal expression of proto-oncogenes

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